NDC neurobiological model: chronic SNS-HPA axis hyperarousal in the first 100 days and stress response settings life-long
Chronic SNS-HPA hyperarousal in very early life is modifiable by environmental factors
In the complex adaptive system of parent and infant, problems of crying and fussing, feeds, and sleep often interact and co-evolve, and may be referred to as ‘regulatory problems’, or ‘dysregulation’.
The neurobiological model of cry-fuss problems conceptualises problem crying as a behavioral biomarker of chronic SNS-HPA hyperarousal, that is, of stress in very early life.20, 21 Crying and fussing, or chronic SNS-HPA hyperarousal, emerge when the parent-infant complex adaptive system is unable to stabilize multiple feedback-loop disruptions arising from interacting and co-evolving environmental factors.21
The neurobiological model of cry-fuss behaviors identifies three key environmental causes of chronic SNS-HPA hyperarousal in the first 100 days post-term:
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Suboptimal environmental stimulation
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First wave behavioral (FWB) approaches to infant sleep
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Unidentified and unmanaged feeding problems, either
a. Poor satiety
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due to compromised milk transfer in breastfeeding, typically due to suboptimal fit and hold (‘latch and positioning’)
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due to feed-spacing in either breast or formula-fed infants
b. Functional lactose overload in breastfed infants
c. Conditioned SNS-HPA hyperarousal with feeds, most often due to positional instability at the breast, or coercive practices with bottle feeds.20
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Key environmental factors interact with monaminergic excitability in the first 100 days predisposing to chronic SNS-HPA hyperarousal
In the neurobiological model of cry-fuss problems, these disruptive environmental factors interact unpredictably in the context of monoaminergic excitability in the first 100 days of life and predispose to:
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High levels of SNS-HPA arousal, which temporarily trigger more SNS-HPA arousal, in a positive feedback loop of inconsolable crying (correlating with monoaminergic excitability);
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Development of conditioned SNS-HPA hyperarousal in response to particular triggers e.g. conditioned SNS-HPA hyperarousal with breastfeeding or bottle-feeding;
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Temporary re-setting of the baby’s ‘stress thermostat’ in response to chronically high levels of SNS-HPA arousal (also known as ‘difficulty shifting arousal states’), which resolves at the end of the crying period;
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Permanent re-calibration of the ‘stress thermostat’ in biologically susceptible infants (that is, permanent alteration of neural connectivity), due to:
a. Alteration of the infant’s stress response settings, and/or
b. Cascade effects of altered parent-infant interactions;
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Maternal chronic SNS-HPA hyperarousal in response to infant crying, feed, and sleep problems, which increases the risk of:
a. Postnatal anxiety and/or depression
b. Avoidance behaviors.20
Chronic SNS-HPA hyperarousal in very early life permanently alters stress response settings in susceptible infants
Multiple studies link infant regulatory problems in the domains of feed, cry-fuss behaviors and sleep with impaired developmental and behavioral outcomes in later childhood. This association is strongest if there is more than one regulatory problem, or if the regulatory problem persists beyond 4-5 months of age.22-33
Regulatory problems in infancy have also been linked with avoidant adult personality traits.34 Multiple persistent regulatory problems are associated with attention problems in later childhood, and trajectories of attention problems from childhood to adulthood.32 A comparative study which claims to show no link between regulatory problems in the first 3 months of life and behavior problems at 2-3 years of age retrospectively excludes infants whose crying was found to persist at 6 months of age.35
Yet it is not possible to predict which infants with cry-fuss problems in very early life will have persistent crying at 5 or 6 months of age, and intervention should be offered promptly to all parents reporting problem crying.
More ‘cued care’ at term predicts fewer regulatory problems at three months, but after the first highly neuroplastic 100 days, patterns of chronic SNS-HPA hyperarousal may become entrenched in susceptible infants, since cued care beyond this age does not result in less regulatory problems. Biological vulnerabilities such as preterm birth provide more significant prediction of long-term regulatory problems.36 But upregulated infant behavior, or crying and fussing, also predisposes to negative affect and mood problems in parents,37, 38 which disrupt the parent’s capacity to engage and lengthen reciprocity chains. This bi-directional disruption to parent-infant biobehavioral synchrony adds to allostatic load in infants.
These findings corroborate the neurobiological model of infant crying, which argues that while most families are resilient, and suffer no long-term effects of excessive infant crying, cry-fuss problems are a behavioral biomarker of infant stress and disrupted parent-infant biobehavioral synchrony due to modifiable environmental factors, and affect the infant’s capacity to attend to developmental tasks. In a small but important subset of genetically susceptible infants or psychosocially vulnerable families, cry-fuss problems are then associated with long-term SNS-HPA axis disruption and developmental impairment.22-33
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